ArticleCell host & microbe2013
Induction of bone loss by pathobiont-mediated Nod1 signaling in the oral cavity.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
94 citing papers in PubMed, 129 citations in OpenAlex.
- Exacerbation of inflammatory bone loss in TET2-driven clonal hematopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- IL-22 synergizes with IL-17 to promote mucosal inflammation and bone loss.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Maternal antibodies regulate the establishment of murine oral and salivary mucosal immunity.Nature communications · 2026Article
- Upregulation of senescence-associated gene expression levels in human gingival tissue affected by periodontitis.Journal of periodontology · 2026Article
- Inflammasome targeting for periodontitis prevention is sex dependent.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The dual roles of peptidoglycans: NOD1 and NOD2 inversely regulate bone metabolism.Experimental & molecular medicine · 2025Article
- Transmission of maternal oral pathobionts to the infant gut predisposes offspring to exacerbated enteritis.Cell reports · 2025Article
- Periodontitis-induced neuroinflammation triggers IFITM3-Aβ axis to cause alzheimer's disease-like pathology and cognitive decline.Alzheimer's research & therapy · 2025Article
- DAMPs, PAMPs, NLRs, RIGs, CLRs and TLRs - Understanding the Alphabet Soup in the Context of Bone Biology.Current osteoporosis reports · 2025Review
- Article
- Osteocyte RANKL Drives Bone Resorption in Mouse Ligature-Induced Periodontitis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- The Complement-Targeted Inhibitor Mini-FH Protects against Experimental Periodontitis via Both C3-Dependent and C3-Independent Mechanisms.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Illuminating the oral microbiome and its host interactions: animal models of disease.FEMS microbiology reviews · 2023Review
- Dysregulation of Stress-Induced Translational Control byMicroorganisms · 2023Article
- Roles of bacterial extracellular vesicles in systemic diseases.Frontiers in microbiology · 2023Review
- Activation of the pattern recognition receptor NOD1 in periodontitis impairs the osteogenic capacity of human periodontal ligament stem cells via p38/MAPK signalling.Cell proliferation · 2022Article
- Oral biofilm dysbiosis during experimental periodontitis.Molecular oral microbiology · 2022Article
- Complement Is Required for Microbe-Driven Induction of Th17 and Periodontitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Interferon activated gene 204 protects against bone loss in experimental periodontitis.Journal of periodontology · 2022Article
- Apitherapy and Periodontal Disease: Insights into In Vitro, In Vivo, and Clinical Studies.Antioxidants (Basel, Switzerland) · 2022Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Periodontitis is a common disease that is characterized by resorption of the alveolar bone and mediated by commensal bacteria that trigger host immune responses and bone destruction through unidentified mechanisms. We report that Nod1, an innate intracellular host receptor for bacterial peptidoglycan-related molecules, is critical for commensal-induced periodontitis in a mouse model. Mice lacking Nod1 exhibit reduced bone resorption as well as impaired recruitment of neutrophils to gingival tissues and osteoclasts to the alveolar bone, which mediate tissue and bone destruction. Further analysis showed that accumulation of a Nod1-stimulating commensal bacterium, NI1060, at gingival sites was sufficient to induce neutrophil recruitment and bone resorption. Genomic sequencing revealed that NI1060 is a mouse-specific bacterium that is related to bacteria associated with the development of aggressive periodontitis in humans. These findings provide insight into commensal-host interactions contributing to periodontitis and identify a potential target for preventing this common oral disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.